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Journal Article

An AP2 transcription factor is required for a sleep-active neuron to induce sleep-like quiescence in C. elegans.

MPS-Authors
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Lewandrowski,  I. L.
Research Group of Sleep and Waking, MPI for biophysical chemistry, Max Planck Society;

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Bringmann,  H.
Research Group of Sleep and Waking, MPI for biophysical chemistry, Max Planck Society;

Fulltext (public)

1868206.pdf
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Supplementary Material (public)

1868206_Suppl_1.pdf
(Supplementary material), 2MB

1868206-Suppl-2.mp4
(Supplementary material), 10MB

1868206-Suppl-3.mp4
(Supplementary material), 24MB

1868206-Suppl-4.mp4
(Supplementary material), 10MB

1868206-Suppl-5.mp4
(Supplementary material), 14MB

Citation

Turek, M., Lewandrowski, I. L., & Bringmann, H. (2013). An AP2 transcription factor is required for a sleep-active neuron to induce sleep-like quiescence in C. elegans. Current Biology, 23(22), 2215-2223. doi:10.1016/j.cub.2013.09.028.


Cite as: http://hdl.handle.net/11858/00-001M-0000-0014-C6E6-D
Abstract
Background: Sleep is an essential behavior that is found in all animals that have a nervous system. Neural activity is thought to control sleep, but little is known about the identity and the function of neural circuits underlying sleep. Lethargus is a developmentally regulated period of behavioral quiescence in C. elegans larvae that has sleep-like properties. Results: We studied sleep-like behavior in C. elegans larvae and found that it requires a highly conserved AP2 transcription factor, aptf-1, which was expressed strongly in only five interneurons in the head. Expression of aptf-1 in one of these neurons, the GABAergic neuron RIS, was required for quiescence. RIS was strongly and acutely activated at the transition from wake-like to sleep-like behavior. Optogenetic activation of aptf-1-expressing neurons ectopically induced acute behavioral quiescence in an aptf-1-dependent manner. RIS ablation caused a dramatic reduction of quiescence. RIS-dependent quiescence, however, does not require GABA but requires neuropeptide signaling. Conclusions: We conclude that RIS acts as a sleep-active, sleep-promoting neuron that requires aptf-1 to induce sleep-like behavior through neuropeptide signaling. Sleep-promoting GABAergic-peptidergic neurons have also been identified in vertebrate brains, suggesting that common circuit principles exist between sleep in vertebrates and sleep-like behavior in invertebrates.